TOO SWEET TOO STORMY PRESENTOR: Dr. Abhinaya PG I (M.D Paeds) CONSULTANTS: Dr. Saji James Dr. J. Dhivyalakshmi Dr. P. N. Vinoth Unit IV, Dept. Of Paediatrics, SRMC & RI
14year old female complaints of Difficulty in breathing 2 days drowsiness and vomiting
HOPI Polyuria - 15 days Diagnosed outside as Type 1 Diabetes Mellitus. Started on insulin(h. Mixtard 10units BD) Compliance poor No h/o fever/cough/loose stools/ burning micturition/ exanthematous illness Birth History: Nil significant Family history of Type 2 DM (+)
IN THE ER (Examination): Drowsy; GCS- 14/15, afebrile PR: 128/min; RR: 48/min; Acidotic breathing+ severe dehydration(+); BP: 90/60mmHg BMI: 13.51(<5 th percentile) SMR: B4 P4 A3 Provisional Diagnosis: DKA INVESTIGATIONS: CBG was HIGH (RBS 664 mg/dl) ph- 6.99, HCO3-3.5 meq/l Urine ketones- +++ Child was given 10ml/kg NS and shifted to PICU
CBG (mg/dl) 1 st hour HIGH (RBS - 664) Fluids (NS) ph HCO3- GCS Others 126ml/hr 6.99 3.5 14/15 Insulin infusion started (0.1 U/kg/hr) 6 hours 630 126 ml/hr 6.89 1.4 12/15 Insulin dose and administration checked. 10 ml/kg NS bolus given. Antibiotics started. 9 hours 600 126 ml/hr 6.98 1.8 10/15 12 hours 560 126 ml/hr 6.88 1.4 7/15 Started on mannitol and intubated (Cerebral edema) Bicarbonate started 24 hours 512 126 ml/hr 6.87 2.6 8T/15 Persistent hypotension. Inotropes - Started. Mannitol stopped & Hypertonic saline started 30 hours 500 126 ml/hr 7.151 5 8T/15 36 hours 490 126 ml/hr 7.182 5.7 8T/15 48 hours 286 126 ml/hr 7.43 9.2 10T/15
Day 1 Day 2 Day 3 RBS 664 500 286 BUN 13 43 37 CREATININE 1.5 3.5 2.7 Urine output 1 ml/kg/hr (progressed to anuria) 0.5 ml/kg/hr (Hemodialysis) Na 130 150 148 K+ 5.4 2.9 3.4 HCO3-4 8 13 Chloride 102 122 115 0.8 ml/kg/hr AKI (Rhabdomyolysis, Shock) underwent 8 cycles of hemodialysis Hypertension (AKI) developed PRES, seizures Controlled with Nifedipine & Phenytoin Had Septic shock (Morganella & Enterococci) and antibiotics given
COURSE IN THE HOSPITAL ( DAY 2) Severe ischemic changes over pressure areas (gluteal, face, occiput, heel) due to persistent shock. Progressed to large ulcers daily dressings done
COURSE IN THE HOSPITAL DAY 2: Hypophosphatemia Proximal muscle weakness and B/L foot drop In view of persistent shock Cortisol 14.44 µg/dl(normal) Hydrocortisone - started in view of persistent shock Tracheostomy for prolonged ventilation Shock slowly resolved (Day 3-5) Conscious level gradually improved (D15 of admission)
As shock resolved Oral feeds started Insulin infusion stopped and subcutaneous insulin started child was gradually weaned off from ventilator support (D20) Tracheostomy wound closed (D60) Steroids were tapered
Planned for Split Skin Graft for the ulcers. Incidentally noticed to have thrombocytosis which gradually progressed (9.5 lakhs/cu.mm). Ruled out - Micro and macro vascular complications, iron deficiency anemia Thrombocytosis- reactive [? stress (large ulcers)/ steroid induced] Steroids withdrawn gradually, however thrombocytosis persisted Stress induced thrombocytosis (large ulcers) Child was taken up for SSG Post-surgery platelet count normalized (4 lakhs/cu.mm)
PROBLEMS INTERVENTIONS DAY RESOLVED DKA Fluids, Insulin Day 3 Cerebral Edema Septic shock (Morganella & Enterococci) AKI & Rhabdomyolysis Hypertension & PRES Mannitol/ 3% Saline, Ventilation Fluids, inotropes, IV Antibiotics Day 5 Day 5-15 8 cycles Hemodialysis Day 5 Antihypertensives & Antiepileptics Pressure Sore/ Ulcer Dressing, Antibiotics, SSG Day 5 Day 120 Foot Drop (CIP) Foot Splint Persisting Reactive thrombocytosis Stress induced Post SSG Total stay in hospital: 120 days
Follow up Sugars are under control HbA1C 6.5 Wound healing (+) Mild residual foot drop (+) Foot splint No sequelae of Cerebral edema
Cerebral Edema: Risk Factors Younger age (e.g., infants and children < 5 years) New-onset diabetes High glucose levels Severe dehydration (elevated BUN/creatinine) Severe acidosis (lower ph, HCO3, pco2) Treatment with bicarbonate Cerebral edema has a significant mortality (24%) and morbidity (35% of survivors) The risk and outcome of cerebral oedema developing during diabetic ketoacidosis Edge JA et al. Arch Dis Child 2001; 85 :16 22
SEPTIC SHOCK IN DKA certain patients, particularly those with complicating illness septic shock, pancreatitis may require more than 20 ml/kg of fluid resuscitation in the first treatment hour and more than 50 ml/kg in the first four hours Physiologic management of DKA G D Harris, I Fiordalisi Arch Dis Child 2002;87:451-452
Poovazhagi V, Prabha Senguttuvan, Padmaraj R Diabetic Clinic, Institute of Child Health and Hospital for Children, Chennai OUTCOME OF ACUTE RENAL FAILURE IN CHILDREN WITH DIABETIC KETO ACIDOSIS (DKA) Of the 130 DKA episodes treated at the Pediatric Intensive Care Unit (PICU), 15 children (11.5%) had renal failure. Sepsis and shock were the common etiological factors. Mortality in ARF complicating DKA was 40%. Persistent acidosis requiring bicarbonate therapy, reduction in intravenous fluid volume, reduced dose of insulin and peritoneal dialysis were the modifications in the treatment for this life-threatening complication. Poovazhagi V, Prabha Senguttuvan, Padmaraj R Department of Pediatric Intensive Care, Institute of Child Health and Hospital for Children, Egmore, Chennai, India UNUSUAL CAUSE OF RENAL FAILURE IN A CHILD WITH DIABETIC KETOACIDOSIS A previously normal 11 year old male child presented with features of diabetic ketoacidosis (DKA) to our pediatric intensive care unit. He had persistent hypokalemia and raised urea, creatinine despite adequate fluid management and insulin. Investigations revealed very high creatinine phosphokinase (CPK) levels suggesting rhabdomyolysis. He developed acute renal failure (ARF) secondary to rhabdomyolysis and recovered completely following supportive management
HIGHLIGHTS 1. Close monitoring of GCS & Urine output Early detection of Cerebral edema & AKI 2. High creatinine at diagnosis and non resolution of acidosis - markers of impending renal failure 3. Persistent metabolic acidosis Think of alternate causes AKI, Sepsis, Rhabdomyolysis, etc., 4. Extubation failure Hypophosphatemia Role of IV phosphate 5. Major morbidity -Pressure ulcers Role of alpha beds in ICU 6. Complete recovery is still possible in stormy DKA - with continuous monitoring, insulin and supportive care.
ACKNOWLEDGEMENTS Dr. Shuba, Dr. Rajkumar & PICU Team Dr. Prabha Senguttuvan & Team - Nephrology